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Related Concept Videos

Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
Cerebrospinal Fluid01:21

Cerebrospinal Fluid

Cerebrospinal fluid (CSF) is a colorless liquid that flows around the brain and the spinal cord, playing a vital role in the protection, support, and overall function of the central nervous system (CNS). CSF production, circulation, and absorption are tightly regulated processes essential for the brain and spinal cord to function properly.
CSF Production
CSF is produced mainly in the choroid plexus, a network of capillaries and ependymal cells located within the ventricular system of the brain.
Increased Intracranial Pressure l: Introduction01:14

Increased Intracranial Pressure l: Introduction

Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
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Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...

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Related Experiment Video

Updated: Jul 16, 2026

3D Modeling of the Lateral Ventricles and Histological Characterization of Periventricular Tissue in Humans and Mouse
15:26

3D Modeling of the Lateral Ventricles and Histological Characterization of Periventricular Tissue in Humans and Mouse

Published on: May 19, 2015

Ventricular cerebrospinal fluid neurofilament protein levels decrease in parallel with white matter pathology after

M Tullberg1, K Blennow, J-E Månsson

  • 1Institute of Clinical Neuroscience, The Sahlgrenska Academy, Göteborg University, Göteborg, Sweden. mats.tullberg@neuro.gu.se

European Journal of Neurology
|March 16, 2007
PubMed
Summary

Normal pressure hydrocephalus (NPH) involves cerebrospinal fluid (CSF) issues and white matter lesions. Shunt surgery improved patient outcomes, linked to reduced axonal markers and white matter changes.

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3D Modeling of the Lateral Ventricles and Histological Characterization of Periventricular Tissue in Humans and Mouse
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Area of Science:

  • Neuroscience
  • Neurology
  • Biochemistry

Background:

  • Normal pressure hydrocephalus (NPH) presents with altered cerebrospinal fluid (CSF) dynamics and white matter lesions (WML).
  • The biochemical underpinnings of NPH-related white matter hyperintensities (PVH) remain largely unexplored.
  • Understanding these biochemical changes is crucial for NPH diagnosis and treatment.

Purpose of the Study:

  • To investigate the biochemical markers in CSF related to periventricular white matter hyperintensities (PVH) in NPH patients.
  • To explore the association between CSF markers, PVH, and clinical outcomes post-shunt surgery.
  • To elucidate the biochemical changes occurring after CSF shunting in NPH.

Main Methods:

  • Analysis of 10 CSF markers, 12 clinical symptoms, and MRI-assessed PVH and ventricular size in 35 NPH patients before and after shunt surgery.
  • Correlation analysis between ventricular CSF neurofilament protein (NFL) and PVH extent.
  • Assessment of changes in CSF markers and clinical status 3 months post-surgery.

Main Results:

  • Elevated ventricular CSF neurofilament protein (NFL) correlated with more extensive PVH.
  • Greater postoperative reduction in NFL was associated with reduced PVH and improved clinical outcomes.
  • Postoperative changes included increases in albumin ratio, HMPG, NPY, VIP, and GD3, and decreases in NFL, tau, and HVA.

Conclusions:

  • NPH involves ongoing periventricular neuronal dysfunction, evidenced by PVH on MRI.
  • Clinical improvement after shunting correlates with restored axonal function indicated by CSF marker changes.
  • Shunting also impacts neurotransmission, blood-brain barrier function, and gliosis in NPH patients.